Pigmentary glaucoma is caused by an overwhelming of the trabecular meshwork by pigment that originates from the posterior surface of the iris. Recent investigations by the proposed principal investigator suggested that the cause of the loss of pigment is a mechanical rubbing between the posterior surface of the iris and anterior packets of zonules in predisposed eyes with generally concave peripheral irides. The studies indicated that when the peripheral iris was flat, contact was unlikely. Miotics, both parasympathomimetics (Pilocarpine) and alpha-adrenergic blocking agents (Thymoxamine) flatten the peripheral iris in these eyes, lifting the peripheral iris away from the zonules. This stops the loss of pigment and stops the continuous insult to the trabecular meshwork allowing, in some cases, the trabecular meshwork to recover normal function. Pilocarpine is a safe drug to use to stop the pigmentary insult, but accommodative blurring is disabling to the often young patients. Thymoxamine, which causes no blurring, would therefore be an ideal miotic agent to use to interrupt this cycle. A clinical trial is proposed. In the laboratory, further study of the pathophysiology of pigmentary glaucoma will be conducted with constant pressure perfusion studies with pigment infusion into enucleated eyes. These studies will be correlated with an attempt to create an animal model for pigmentary glaucoma in monkeys. The role of phagocytosis of the endothelial cells lining the trabecular meshwork in the creation and cure of secondary and primary open angle glaucoma is poorly understood. No one has evaluated the possible therapeutic effect of macrophages, injected into living eyes, upon these glaucomas. If an animal model of a secondary glaucoma, pigmentary glaucoma, can be established, macrophages will be injected into the anterior chamber of these living eyes to determine if there is a beneficial effect.